The goal of this study is to determine the role of pulmonary metabolism of essential fatty acids, e.g., arachidonic acid in the etiology of intra-arterial thrombosis. This study will determine the factors controlling production of prostaglandins and thromboxanes by pulmonary tissue and vascular endothelium. We have found that respiration rate influences the pulmonary production of PGI2 and TXA2. Increasing the respiration rate preferentially stimulates PGI2 biosynthesis. The presence of platelets or platelet membranes in the vascular bed acts as a stimulator of membrane phospholipase, liberating arachidonic acid and resulting in an increased release of PGI2 from the lung. Using in vitro systems, we have studied the role of peroxidase in control of PGI2 biosynthesis. Chemicals that stimulate the peroxidase reduce levels of hydroperoxides that inhibit PGI2 biosynthesis, resulting in a stimulation of PGI2 production.